Gilhar Amos, Landau Marina, Assy Bedia, Shalaginov Raya, Serafimovich Sima, Kalish Richard S
Research Laboratories, Flieman Medical Center and B. Rappaport Faculty of Medicine, Technion Institute of Technology, Haifa, Israel.
Arch Dermatol. 2002 Jul;138(7):916-22. doi: 10.1001/archderm.138.7.916.
To determine the role of CD4+ and CD8+ T lymphocytes in the pathogenesis of alopecia areata.
Relapse of alopecia areata was induced in autologous human scalp grafts on Prkdc(scid) mice by injection of activated T lymphocytes derived from lesional skin. CD4+ and CD8+ T cells were separated by magnetic beads before injection.
University-based dermatology practice.
Eleven patients with either alopecia totalis or severe alopecia areata.
Hair regrowth, hair loss, and immunohistochemical findings of scalp explants.
Transfer of scalp T cells to autologous lesional scalp explants on Prkdc(scid) mice.
Injection of unseparated T cells and mixed CD4+ plus CD8+ T cells resulted in significant hair loss (P<.01) in 5 of 5 experiments. However, injection of purified CD4+ or CD8+ T cells alone did not result in reproducible hair loss. CD4+ and CD8+ T cells induced follicular expression of intercellular adhesion molecule 1 (CD54), HLA-DR, and HLA-A, HLA-B, and HLA-C after injection into scalp grafts.
CD4+ and CD8+ T cells have a role in the pathogenesis of alopecia areata. It is hypothesized that CD8+ T cells act as the effector cells, with CD4+ T cell help. It is now necessary to look for HLA-A, HLA-B, and HLA-C associations with alopecia areata. Therapeutic manipulations that interfere with CD8+ activity should be examined.
确定CD4+和CD8+ T淋巴细胞在斑秃发病机制中的作用。
通过注射来自皮损处皮肤的活化T淋巴细胞,在Prkdc(scid)小鼠的自体人头皮移植片上诱导斑秃复发。注射前通过磁珠分离CD4+和CD8+ T细胞。
大学皮肤科诊所。
11例全秃或重度斑秃患者。
毛发再生、脱发情况以及头皮外植体的免疫组化结果。
将头皮T细胞转移至Prkdc(scid)小鼠的自体皮损头皮外植体上。
在5项实验中的5项中,注射未分离的T细胞以及混合的CD4+加CD8+ T细胞导致显著脱发(P<0.01)。然而,单独注射纯化的CD4+或CD8+ T细胞并未导致可重复的脱发。注射到头皮移植片中后,CD4+和CD8+ T细胞诱导了细胞间黏附分子1(CD54)、HLA-DR以及HLA-A、HLA-B和HLA-C的毛囊表达。
CD4+和CD8+ T细胞在斑秃发病机制中起作用。据推测,CD8+ T细胞在CD4+ T细胞的辅助下作为效应细胞发挥作用。现在有必要寻找斑秃与HLA-A、HLA-B和HLA-C的关联。应研究干扰CD8+活性的治疗方法。